NU 665D Final exam
1. INR interpretation: -No anticoagulation therapy level: should be ~1.0
-Higher the number, greater risk of bleeding
-Anticoagulation therapy target level: 2.0-4.0
-INRs >5 avoided d/t risk of bleed
2. Treatment Approach to A. Fib: 3 Elements:
1) Rate control
2) Restoration and maintenance of sinus rhythm (if indicated)
3) Stroke prevention
-Goal is to alleviate sxs and improve QOL
3. Rhythm Control: Focus on restoration of sinus rhythm:
-Palpitations
-SOB
-Dizziness/Lightheadedness
-Activity intolerance
Prevention of tachycardia-induced cardiomyopathyPrevention of hemodynamic compromise
r/t A.Fib
4. Rhythm Control Treatment: Specific tx type depends on several factors:
-Heart disease w/LVH or depressed LVEF
-HF
-Age
-Underlying sinus node dysfunction
-Other arrhythmias (e.g. a. flutter)
-Underlying QT prolongation
-Renal function
Note: pts w/a CHADS2VASc2 score of zero who opt for a rhythm control strategymay be
considered to stop OAC
5. Pharmacologic Management of A. Fib: Class 1: Na+ channel blockers, Quini-dine,
Procainamide, Disopyramide, Lidocaine, Mexilitine, Flecainide, PropafenoneClass 2: Beta
Blockers
,Class 3: K+ channel blockers, Sotalol, Amiodarone, Dofetilide, Dronedarone
6. Side Effects of A. Fib Drugs: -Amiodarone Toxicity: pulmonary, thyroid, liver,
photosensitivity, skin discoloration
-QT Prolongation
-Avoid QT prolonging meds
7. Ablation Procedure: -Pulmonary vein Isolation (LA)
-Radiofreq. ablation
-Not curative, but sign. reduces the amount of A. Fib
-General anesthesia, groin access
-Generally reserved for pts who have failed at least one attempt at DC cardioversion,1 or 2
antiarrhythmic agents
8. Rate Control: General goal: 60-80 BPM at restNot all pts req drug therapy for this
Tx with: BB (metoprolol, atenolol, carvidolol (HF), Non-dihydropyridine CCB (dilti-azem,
verapamil), Digoxin (not 1st line)
Consider co-morbidities: HF (non-dihydropyrodine CCB should not be used in HFwith low
EF d/t negative ionotropic effect; LVEF
-Rate control strategy can be appropriate for older pts who are more prone to druginteractions
and are asymptomic in A.Fib
9. Heart failure: Inability of the heart to provide forward output to meet the perfu-sion and
oxygenation requirements while maintaining normal filling pressures
10. Systolic Dysfunction: Impaired cardiac contractile function
-Majority of heart failure cases
-Left or right sided
-Abnormalities in the systolic function
-Reduced LVEF often <50%
-Progressive chamber dilation
11. Diastolic Function: Abnormal cardiac relaxation, stiffness or filling
-Normal LVEF
-Often dx'd when pts present w/HF sxs and preserved LVEF
-Often hypertrophic w/impaired relaxation
-Longstanding uncontrolled HTN
12. Left Sided Heart Failure: -Often presents w/pulmonary edema, fluid backing upin
,pulmonary circuit
-Decreased contracility and cardiac output
-Compensatory increase in catecholamines to drive up cardiac output
-Catecholamin increase causes increased BP
-Laterally displaced apical pulse
-S3 Gallop rhythm
13. Right Sided Heart Failure: Presents w/systemic edema:
-JVD
-Leg edema
-Hepatosplenomegaly
Left sided HF is most common causeChronic lung disease
Elevated JVD (hepatojugular reflux)LE edema
Poor perfsuon
-poor capillary refill
-cool distal extremities
14. AHA Definition of Heart Failure: -HF with reduced EF: EF</= 40% (HFrEF)
-HF with preserved EF: EF >/= 50% (HFpEF)
-Borderline HFpEF, EF 41-49%
15. AHA Guidelines for Heart Failure: -Continuously address risk factors (HTN,lipids,
obesity, DM, tobacco)
-Mortality benefit from using guideline-directed medical therapy
-Anticoagulation should not be used in pts w/chronic HFrEF w/no risk factors
-Aim for control of systolic and diastolic BPs, as well as volume stats, to tx HFrEF
-HF education, dietary restrictions, exercise training
-HF multidisciplinary team including palliative care should be provided involvedwhen tx-ing
pts w/advanced HF
16. Causes of Heart Failure: -CAD
-MI- 15-fold increased risk, single most potent risk factor for developing HF
-HTN (major cause of diastolic dysfunction)
-Valvular heart disease: Ventricular remodeling
, -Cardiomyopathy
-LVH
-DM
-Dyslipidemia
-Cocaine abuse
-Exposure to cardiotoxic agents- chemo
17. Atrial Fibrillation: Irregularly irregular rhythm
-Absence of discernible P wave
-Atrial disorganization
18. Paroxysmal A. Fib: -Recurrent
>1 episode lasting 30 or more seconds in durationAF that terminates spontaneously within 7
days
19. Persistent A. Fib: Sustained A. Fib >7 days ORLasts <7 days but requires cardioversion
20. Permanent A. Fib: Refractory to cardioversion or accepted as a final rhythm
21. Acute A. Fib: New onset OR first episode of A. Fib
22. Lone A. Fib: patients <60yo without evidence of cardiac, pulmonary or circulatorydisease
23. A. Fib Associated Cardiac Conditions: -HTN
-CHF
-CAD
-Rheumatic valvular disease
-Atrial and ventricular dilation or hypertrophy
-Congential heart disease
24. A. Fib Associated Non-Cardiac Conditions: -Thyroid disease
-ETOH and caffeine abuse
-Pulmonary HTN
-COPD, OSA
-Infections
-Family/genetics (rare cases)
25. Clinical Presentation of A. Fib: -Palpitations, tachycardia
-Fatigue
1. INR interpretation: -No anticoagulation therapy level: should be ~1.0
-Higher the number, greater risk of bleeding
-Anticoagulation therapy target level: 2.0-4.0
-INRs >5 avoided d/t risk of bleed
2. Treatment Approach to A. Fib: 3 Elements:
1) Rate control
2) Restoration and maintenance of sinus rhythm (if indicated)
3) Stroke prevention
-Goal is to alleviate sxs and improve QOL
3. Rhythm Control: Focus on restoration of sinus rhythm:
-Palpitations
-SOB
-Dizziness/Lightheadedness
-Activity intolerance
Prevention of tachycardia-induced cardiomyopathyPrevention of hemodynamic compromise
r/t A.Fib
4. Rhythm Control Treatment: Specific tx type depends on several factors:
-Heart disease w/LVH or depressed LVEF
-HF
-Age
-Underlying sinus node dysfunction
-Other arrhythmias (e.g. a. flutter)
-Underlying QT prolongation
-Renal function
Note: pts w/a CHADS2VASc2 score of zero who opt for a rhythm control strategymay be
considered to stop OAC
5. Pharmacologic Management of A. Fib: Class 1: Na+ channel blockers, Quini-dine,
Procainamide, Disopyramide, Lidocaine, Mexilitine, Flecainide, PropafenoneClass 2: Beta
Blockers
,Class 3: K+ channel blockers, Sotalol, Amiodarone, Dofetilide, Dronedarone
6. Side Effects of A. Fib Drugs: -Amiodarone Toxicity: pulmonary, thyroid, liver,
photosensitivity, skin discoloration
-QT Prolongation
-Avoid QT prolonging meds
7. Ablation Procedure: -Pulmonary vein Isolation (LA)
-Radiofreq. ablation
-Not curative, but sign. reduces the amount of A. Fib
-General anesthesia, groin access
-Generally reserved for pts who have failed at least one attempt at DC cardioversion,1 or 2
antiarrhythmic agents
8. Rate Control: General goal: 60-80 BPM at restNot all pts req drug therapy for this
Tx with: BB (metoprolol, atenolol, carvidolol (HF), Non-dihydropyridine CCB (dilti-azem,
verapamil), Digoxin (not 1st line)
Consider co-morbidities: HF (non-dihydropyrodine CCB should not be used in HFwith low
EF d/t negative ionotropic effect; LVEF
-Rate control strategy can be appropriate for older pts who are more prone to druginteractions
and are asymptomic in A.Fib
9. Heart failure: Inability of the heart to provide forward output to meet the perfu-sion and
oxygenation requirements while maintaining normal filling pressures
10. Systolic Dysfunction: Impaired cardiac contractile function
-Majority of heart failure cases
-Left or right sided
-Abnormalities in the systolic function
-Reduced LVEF often <50%
-Progressive chamber dilation
11. Diastolic Function: Abnormal cardiac relaxation, stiffness or filling
-Normal LVEF
-Often dx'd when pts present w/HF sxs and preserved LVEF
-Often hypertrophic w/impaired relaxation
-Longstanding uncontrolled HTN
12. Left Sided Heart Failure: -Often presents w/pulmonary edema, fluid backing upin
,pulmonary circuit
-Decreased contracility and cardiac output
-Compensatory increase in catecholamines to drive up cardiac output
-Catecholamin increase causes increased BP
-Laterally displaced apical pulse
-S3 Gallop rhythm
13. Right Sided Heart Failure: Presents w/systemic edema:
-JVD
-Leg edema
-Hepatosplenomegaly
Left sided HF is most common causeChronic lung disease
Elevated JVD (hepatojugular reflux)LE edema
Poor perfsuon
-poor capillary refill
-cool distal extremities
14. AHA Definition of Heart Failure: -HF with reduced EF: EF</= 40% (HFrEF)
-HF with preserved EF: EF >/= 50% (HFpEF)
-Borderline HFpEF, EF 41-49%
15. AHA Guidelines for Heart Failure: -Continuously address risk factors (HTN,lipids,
obesity, DM, tobacco)
-Mortality benefit from using guideline-directed medical therapy
-Anticoagulation should not be used in pts w/chronic HFrEF w/no risk factors
-Aim for control of systolic and diastolic BPs, as well as volume stats, to tx HFrEF
-HF education, dietary restrictions, exercise training
-HF multidisciplinary team including palliative care should be provided involvedwhen tx-ing
pts w/advanced HF
16. Causes of Heart Failure: -CAD
-MI- 15-fold increased risk, single most potent risk factor for developing HF
-HTN (major cause of diastolic dysfunction)
-Valvular heart disease: Ventricular remodeling
, -Cardiomyopathy
-LVH
-DM
-Dyslipidemia
-Cocaine abuse
-Exposure to cardiotoxic agents- chemo
17. Atrial Fibrillation: Irregularly irregular rhythm
-Absence of discernible P wave
-Atrial disorganization
18. Paroxysmal A. Fib: -Recurrent
>1 episode lasting 30 or more seconds in durationAF that terminates spontaneously within 7
days
19. Persistent A. Fib: Sustained A. Fib >7 days ORLasts <7 days but requires cardioversion
20. Permanent A. Fib: Refractory to cardioversion or accepted as a final rhythm
21. Acute A. Fib: New onset OR first episode of A. Fib
22. Lone A. Fib: patients <60yo without evidence of cardiac, pulmonary or circulatorydisease
23. A. Fib Associated Cardiac Conditions: -HTN
-CHF
-CAD
-Rheumatic valvular disease
-Atrial and ventricular dilation or hypertrophy
-Congential heart disease
24. A. Fib Associated Non-Cardiac Conditions: -Thyroid disease
-ETOH and caffeine abuse
-Pulmonary HTN
-COPD, OSA
-Infections
-Family/genetics (rare cases)
25. Clinical Presentation of A. Fib: -Palpitations, tachycardia
-Fatigue
